Resveratrol protects intestinal epithelial cells against radiation-induced damage by promoting autophagy and inhibiting apoptosis through SIRT1 activation

Qin, Haoren; Zhang, Heng; Zhu, Siwei; Wang, Hui

doi:10.1093/jrr/rrab035

Cited by 21 publications

(9 citation statements)

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“…Autophagy may partially counteract apoptotic cell death via the cell survival pathway at an earlier stage. Similar results were recently reported in which resveratrol induced SIRT1-dependent autophagy to prevent apoptosis in VSC4.1 motoneurons (Tian et al, 2021), intestinal epithelial cells (Qin et al, 2021) and human trophoblasts (Wang et al, 2020).…”

Section: Discussionsupporting

confidence: 90%

Resveratrol inhibits hepatic stellate cell activation by regulating autophagy and apoptosis through the SIRT1 and JNK signaling pathways

Zhang

Jian

Jiang

et al. 2022

Journal of Food Biochemistry

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Resveratrol, a natural polyphenol found in grapes, berries, peanuts, and medicinal plants, has previously been reported to have several biological activities, including inhibiting hepatic brosis. Hepatic stellate cell (HSC) activation is the major cellular source of matrix protein-secreting myo broblasts, which are the major drivers of liver brogenesis. Numerous studies on the protective effects of resveratrol against liver brosis have focused on the inhibition of HSC activation. Although the underlying mechanisms remain to be fully elucidated, autophagy and apoptosis regulation might be intimately related. The mouse HSC line JS1 was stimulated with resveratrol to assess the mechanism and relationship between autophagy and apoptosis. Resveratrol dose-dependently modulated JS1 cell viability. Moreover, resveratrol inhibited JS1 cell activation and induced autophagy and apoptosis. This anti brotic effect was attenuated when autophagy was inhibited using chloroquine (CQ) or 3-methyladenine (3-MA) or when apoptosis was inhibited using Z-VAD-FMK. Furthermore, whether the Sirtuin1 (SIRT1) and c-Jun N-terminal kinase (JNK) signaling pathways were associated with resveratrol-induced autophagy and apoptosis in JS1 cells was examined. The SIRT1 inhibitor EX527 reversed autophagy, and the JNK inhibitor SP600125 was able to reverse both autophagy and apoptosis induced by resveratrol. These ndings suggest that the SIRT1 and JNK signaling pathways may be involved in resveratrol-mediated inhibition of HSC activation by regulating autophagy and apoptosis. Materials And Methods Cells and cell cultureThe immortalized mouse HSC line JS1 was kindly provided by Professor Scott L. Friedman (Mt. Sinai School of Medicine, USA). JS1 cells were cultured in DMEM (Gibco; Thermo Fisher Scienti c, Inc.) supplemented with 10% FBS (Gibco; Thermo Fisher Scienti c, Inc.) and 1% penicillin/streptomycin at 5% CO 2 and 37°C. The medium was replaced with media supplemented with 0.5% FBS for 12 h prior to treatment. Different concentrations of resveratrol (cat. no. R5010; Sigma) was added to the medium and an incubated for different durations, according to the experimental design. JS1 cells were pretreated with 5 mM 3-methyladenine (3-MA; cat. no. M9281; Sigma-Aldrich; Merck KGaA), 30 µM chloroquine (CQ) diphosphate salt (cat. no. C6628; Sigma-Aldrich; Merck KGaA) or 20 µM Z-VAD-FMK (cat. no. C1202; Beyotime Institute of Biotechnology) for 2 h and 10 µM EX527 (cat. no. ab141506; Abcam) or 10 µM SP600125 (cat. no. ab120065; Abcam) for 1 h, followed by treatment with or without 50 µM resveratrol for 24 h. Each in vitro experiment was repeated three times. Measurement of JS1 cell viabilityCells were plated in plastic 96-well plates and incubated with 0.1, 1, 10, 50 or 100 µM resveratrol for 24 h. Subsequently, cell viability was assessed using an MTT Cell Proliferation and Cytotoxicity Assay kit (cat.

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Section: Discussionsupporting

confidence: 90%

Resveratrol inhibits hepatic stellate cell activation by regulating autophagy and apoptosis through the SIRT1 and JNK signaling pathways

Zhang

Jian

Jiang

et al. 2022

Journal of Food Biochemistry

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“…SIRT1 is an NAD + -dependent deacetylase involved in the regulation of inflammation, oxidative stress, autophagy, DNA damage repair, cell apoptosis, and cellular senescence ( Zeng et al, 2019 ; Guo et al, 2021 ). In recent studies, it was found that SIRT1 could promote autophagy and inhibit apoptosis, thereby attenuating radiation-induced IEC-6 cell damage and preventing hypoxic heart damage ( Luo et al, 2019 ; Qin et al, 2021 ). Furthermore, Ren et al (2019) reported that appropriate up-regulation of SIRT1 expression could promote autophagy and inhibit apoptosis in OGD/R-induced injury, thereby improving cellular tolerance to OGD/R injury.…”

Section: Discussionmentioning

confidence: 99%

Protocatechualdehyde Rescues Oxygen-Glucose Deprivation/Reoxygenation-Induced Endothelial Cells Injury by Inducing Autophagy and Inhibiting Apoptosis via Regulation of SIRT1

et al. 2022

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Background: Oxidative stress-induced endothelial cell death, such as apoptosis and autophagy, plays a critical role in ischemia-reperfusion injury. Protocatechualdehyde (PCA) is a major bioactive component of the traditional Chinese medicine Salvia miltiorrhiza Bunge (Lamiaceae), and it has been proved to be effective in the prevention and treatment of ischemic cardiovascular and cerebrovascular diseases. However, its role in oxidative stress-induced endothelial cell death and its underlying mechanisms remains unclear. This study aims to investigate the effects and mechanisms of PCA on endothelial cell apoptosis and autophagy induced by oxygen-glucose deprivation/reoxygenation (OGD/R) injury.Methods: After OGD/R induction, human umbilical vein endothelial cells (HUVECs) were treated with different concentrations of PCA. Cell viability, apoptosis, and autophagy were detected by Cell Counting Kit-8 assay, flow cytometry, and monodansylcadaverine assay, respectively. Western blot was applied to explore the effects of PCA on the expression levels of relevant protein factors.Results: The results show that PCA significantly promoted cell survival rate and cell proliferation and enhanced the antioxidant activity in OGD/R-induced HUVECs. PCA inhibited HUVECs apoptosis, as evidenced by decreased expression of cleaved-caspase-3, Bcl2-associated X (BAX), and increased expression of Bcl-2. PCA induced autophagy by reducing the expression of P62 while increasing the expression of Beclin-1 and LC3 II/I. Meanwhile, PCA enhanced the expression of Sirtuin 1 (SIRT1) and suppressed the expression of P53. When SIRT1 was inhibited by selisistat or SIRT1 small-interfering RNA, the anti-apoptotic and pro-autophagy abilities of PCA were attenuated.Conclusion: These results demonstrated that PCA rescued HUVECs from OGD/R-induced injury by promoting autophagy and inhibiting apoptosis through SIRT1 and could be developed as a potential therapeutic agent against ischemic diseases.

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“…Another study found that the mRNA levels of TJ-associated proteins were down-regulated in HFD-induced mice, which can be reversed after resveratrol treatment ( 66 ). In addition, resveratrol can prevent porcine intestinal epithelial cells from deoxynivalenol-induced damage through the Nrf2 signaling pathway ( 69 ), and decrease radiation-induced damage in intestinal epithelial cells via facilitating autophagy and preventing apoptosis by the activation of SIRT1 ( 70 ). Meanwhile, resveratrol can alleviate H 2 O 2 -induced damage through upregulating the expression of tight-junction proteins (occludin, claudin-1, and ZO-1), which depends on the PI3K/Akt-mediated Nrf2 signaling pathway ( 71 ).…”

Section: Resveratrol and Intestinal Barriermentioning

confidence: 99%

Resveratrol in Intestinal Health and Disease: Focusing on Intestinal Barrier

Wang

Hong

et al. 2022

Front. Nutr.

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The integrity of intestinal barrier determines intestinal homeostasis, which could be affected by various factors, like physical, chemical, and biological stimuli. Therefore, it is of considerable interest and importance to maintain intestinal barrier function. Fortunately, many plant polyphenols, including resveratrol, could affect the health of intestinal barrier. Resveratrol has many biological functions, such as antioxidant, anti-inflammation, anti-tumor, and anti-cardiovascular diseases. Accumulating studies have shown that resveratrol affects intestinal tight junction, microbial composition, and inflammation. In this review, we summarize the effects of resveratrol on intestinal barriers as well as the potential mechanisms (e.g., inhibiting the growth of pathogenic bacteria and fungi, regulating the expression of tight junction proteins, and increasing anti-inflammatory T cells while reducing pro-inflammatory T cells), and highlight the applications of resveratrol in ameliorating various intestinal diseases.

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Resveratrol protects intestinal epithelial cells against radiation-induced damage by promoting autophagy and inhibiting apoptosis through SIRT1 activation

Cited by 21 publications

References 28 publications

Resveratrol inhibits hepatic stellate cell activation by regulating autophagy and apoptosis through the SIRT1 and JNK signaling pathways

Resveratrol inhibits hepatic stellate cell activation by regulating autophagy and apoptosis through the SIRT1 and JNK signaling pathways

Protocatechualdehyde Rescues Oxygen-Glucose Deprivation/Reoxygenation-Induced Endothelial Cells Injury by Inducing Autophagy and Inhibiting Apoptosis via Regulation of SIRT1

Resveratrol in Intestinal Health and Disease: Focusing on Intestinal Barrier

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